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Infection and Immunity, February 2002, p. 820-825, Vol. 70, No. 2
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.70.2.820-825.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Irene T. Ling,2 Wendy Howard,1 Anthony A. Holder,2 and Eleanor M. Riley1*
Institute of Cell, Animal and Population Biology, Edinburgh University, Edinburgh EH9 3JT,1 National Institute for Medical Research, Mill Hill, London NW7 1AA, United Kingdom2
Received 18 June 2001/ Returned for modification 17 October 2001/ Accepted 5 November 2001
Vaccination of mice with the 42-kDa region of Plasmodium yoelii merozoite surface protein 1 (MSP142) or its 19-kDa C-terminal processing product (MSP119) can elicit protective antibody responses in mice. To investigate if the 33-kDa N-terminal fragment (MSP133) of MSP142 also induces protection, the gene segment encoding MSP133 was expressed as a glutathione S-transferase (GST) fusion protein. C57BL/6 and BALB/c mice were immunized with GST-MSP133 and subsequently challenged with the lethal P. yoelii YM blood stage parasite. GST-MSP133 failed to induce protection, and all mice developed patent parasitemia at a level similar to that in naive or control (GST-immunized) mice; mice immunized with GST-MSP119 were protected, as has been shown previously. Specific prechallenge immunoglobulin G (IgG) antibody responses to MSP1 were analyzed by enzyme-linked immunosorbent assay and immunofluorescence. Despite being unprotected, several mice immunized with MSP133 had antibody titers (of all IgG subclasses) that were comparable to or higher than those in mice that were protected following immunization with MSP119. The finding that P. yoelii MSP133 elicits strong but nonprotective antibody responses may have implications for the design of vaccines for humans based on Plasmodium falciparum or Plasmodium vivax MSP142.
Present address: Mabtech, SE-131 37 Nacka, Sweden.
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